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Monocyte chemotactic protein-1 as a potential biomarker for early anti-thrombotic therapy after ischemic stroke
Inflammation following ischemic brain injury is correlated with adverse outcome. Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein...
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Published in: | International journal of molecular sciences 2012-07, Vol.13 (7), p.8670-8678 |
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description | Inflammation following ischemic brain injury is correlated with adverse outcome. Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. The EARLY trial randomized patients with ischemic stroke or TIA to either ASA + ER-DP treatment or ASA monotherapy within 24 h following the event. After 7 days, all patients were treated for up to 90 days with ASA + ER-DP. MCP-1 was determined from blood samples taken from 425 patients on admission and day 8. The change in MCP-1 from admission to day 8 did not differ between patients treated with ASA + ER-DP and ASA monotherapy (p > 0.05). Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Our data does not provide any evidence that treatment with ASA + ER-DP lowers MCP-1 in acute stroke patients. However, MCP-1 may be a useful biomarker for deciding on early stroke therapy, as patients with high MCP-1 at baseline appear to benefit from early treatment with ASA + ER-DP. |
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Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. The EARLY trial randomized patients with ischemic stroke or TIA to either ASA + ER-DP treatment or ASA monotherapy within 24 h following the event. After 7 days, all patients were treated for up to 90 days with ASA + ER-DP. MCP-1 was determined from blood samples taken from 425 patients on admission and day 8. The change in MCP-1 from admission to day 8 did not differ between patients treated with ASA + ER-DP and ASA monotherapy (p > 0.05). Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Our data does not provide any evidence that treatment with ASA + ER-DP lowers MCP-1 in acute stroke patients. However, MCP-1 may be a useful biomarker for deciding on early stroke therapy, as patients with high MCP-1 at baseline appear to benefit from early treatment with ASA + ER-DP.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms13078670</identifier><identifier>PMID: 22942727</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>acetylsalicylic acid (ASA) ; Adult ; Aged ; Aged, 80 and over ; antithrombotic therapy ; Aspirin ; Aspirin - administration & dosage ; Biomarkers ; Biomarkers - blood ; Body mass index ; Brain Ischemia - blood ; Brain Ischemia - drug therapy ; Chemokine CCL2 - blood ; dipyridamole ; Dipyridamole - administration & dosage ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Humans ; Ischemia ; ischemic stroke ; Leukocytes ; Male ; Middle Aged ; monocyte chemoattractant protein-1 (MCP-1) ; neuroprotection ; Platelet Aggregation Inhibitors - administration & dosage ; Proteins ; Stroke ; Stroke - blood ; Stroke - drug therapy ; Time Factors ; Traumatic brain injury</subject><ispartof>International journal of molecular sciences, 2012-07, Vol.13 (7), p.8670-8678</ispartof><rights>Copyright MDPI AG 2012</rights><rights>2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-3c3d7badbefb7e69bd262a51b6407e124390c856558a11e809c05ff7d148b3413</citedby><cites>FETCH-LOGICAL-c577t-3c3d7badbefb7e69bd262a51b6407e124390c856558a11e809c05ff7d148b3413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1526020470/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1526020470?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22942727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Worthmann, Hans</creatorcontrib><creatorcontrib>Dengler, Reinhard</creatorcontrib><creatorcontrib>Schumacher, Helmut</creatorcontrib><creatorcontrib>Schwartz, Andreas</creatorcontrib><creatorcontrib>Eisert, Wolfgang G</creatorcontrib><creatorcontrib>Lichtinghagen, Ralf</creatorcontrib><creatorcontrib>Weissenborn, Karin</creatorcontrib><title>Monocyte chemotactic protein-1 as a potential biomarker for early anti-thrombotic therapy after ischemic stroke</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Inflammation following ischemic brain injury is correlated with adverse outcome. Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. The EARLY trial randomized patients with ischemic stroke or TIA to either ASA + ER-DP treatment or ASA monotherapy within 24 h following the event. After 7 days, all patients were treated for up to 90 days with ASA + ER-DP. MCP-1 was determined from blood samples taken from 425 patients on admission and day 8. The change in MCP-1 from admission to day 8 did not differ between patients treated with ASA + ER-DP and ASA monotherapy (p > 0.05). Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Our data does not provide any evidence that treatment with ASA + ER-DP lowers MCP-1 in acute stroke patients. However, MCP-1 may be a useful biomarker for deciding on early stroke therapy, as patients with high MCP-1 at baseline appear to benefit from early treatment with ASA + ER-DP.</description><subject>acetylsalicylic acid (ASA)</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>antithrombotic therapy</subject><subject>Aspirin</subject><subject>Aspirin - administration & dosage</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Body mass index</subject><subject>Brain Ischemia - blood</subject><subject>Brain Ischemia - drug therapy</subject><subject>Chemokine CCL2 - blood</subject><subject>dipyridamole</subject><subject>Dipyridamole - administration & dosage</subject><subject>Drug Therapy, Combination</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Ischemia</subject><subject>ischemic stroke</subject><subject>Leukocytes</subject><subject>Male</subject><subject>Middle Aged</subject><subject>monocyte chemoattractant protein-1 (MCP-1)</subject><subject>neuroprotection</subject><subject>Platelet Aggregation Inhibitors - administration & dosage</subject><subject>Proteins</subject><subject>Stroke</subject><subject>Stroke - blood</subject><subject>Stroke - drug therapy</subject><subject>Time Factors</subject><subject>Traumatic brain injury</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqFkk1v1DAQhiMEoqVw44wiceHQgD9j54JUVRQqFXGBszV2Jt1sk3ixvUj775llS7XlwinO-PGj8eupqtecvZeyYx_G9Zy5ZMa2hj2pTrkSomGsNU-P1ifVi5zXjAkpdPe8OhGiU8IIc1rFr3GJYVewDiucY4FQxlBvUiw4Lg2vIddQb-hvKSNMtR_jDOkOUz3EVCOkaVcDbTVlleLs4_5wWWGCDdWHQtyY92Iq55LiHb6sng0wZXx1_z2rflx9-n75pbn59vn68uKmCdqY0sgge-Oh9zh4g23ne9EK0Ny3ihnkQtHNg9Wt1hY4R8u6wPQwmJ4r66Xi8qy6Pnj7CGu3SSO1vXMRRvenENOtg0TdTugCVxCCkhQUKN2i73ro9GCB4vXSILk-HlybrZ-xD5RFgumR9PHOMq7cbfzlJEmFtiR4dy9I8ecWc3EzxYLTBAvGbXZc8U7Sc1j5f5RJY20rjSb07T_oOm7TQqk6rkXLBFOGEXV-oEKKOSccHvrmzO0HyB0PEOFvju_6AP-dGPkbd_DCkg</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Worthmann, Hans</creator><creator>Dengler, Reinhard</creator><creator>Schumacher, Helmut</creator><creator>Schwartz, Andreas</creator><creator>Eisert, Wolfgang G</creator><creator>Lichtinghagen, Ralf</creator><creator>Weissenborn, Karin</creator><general>MDPI AG</general><general>Molecular Diversity Preservation International (MDPI)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120701</creationdate><title>Monocyte chemotactic protein-1 as a potential biomarker for early anti-thrombotic therapy after ischemic stroke</title><author>Worthmann, Hans ; Dengler, Reinhard ; Schumacher, Helmut ; Schwartz, Andreas ; Eisert, Wolfgang G ; Lichtinghagen, Ralf ; Weissenborn, Karin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-3c3d7badbefb7e69bd262a51b6407e124390c856558a11e809c05ff7d148b3413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>acetylsalicylic acid (ASA)</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>antithrombotic therapy</topic><topic>Aspirin</topic><topic>Aspirin - administration & dosage</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Body mass index</topic><topic>Brain Ischemia - blood</topic><topic>Brain Ischemia - drug therapy</topic><topic>Chemokine CCL2 - blood</topic><topic>dipyridamole</topic><topic>Dipyridamole - administration & dosage</topic><topic>Drug Therapy, Combination</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Ischemia</topic><topic>ischemic stroke</topic><topic>Leukocytes</topic><topic>Male</topic><topic>Middle Aged</topic><topic>monocyte chemoattractant protein-1 (MCP-1)</topic><topic>neuroprotection</topic><topic>Platelet Aggregation Inhibitors - administration & dosage</topic><topic>Proteins</topic><topic>Stroke</topic><topic>Stroke - blood</topic><topic>Stroke - drug therapy</topic><topic>Time Factors</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Worthmann, Hans</creatorcontrib><creatorcontrib>Dengler, Reinhard</creatorcontrib><creatorcontrib>Schumacher, Helmut</creatorcontrib><creatorcontrib>Schwartz, Andreas</creatorcontrib><creatorcontrib>Eisert, Wolfgang G</creatorcontrib><creatorcontrib>Lichtinghagen, Ralf</creatorcontrib><creatorcontrib>Weissenborn, Karin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest - 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Preclinical studies indicate that treatment with acetylsalicylic acid + extended-release dipyridamole (ASA + ER-DP) has anti-inflammatory and thereby neuroprotective effects by inhibition of monocyte chemotactic protein-1 (MCP-1) expression. We hypothesized that early treatment with ASA + ER-DP will reduce levels of MCP-1 also in patients with ischemic stroke. The EARLY trial randomized patients with ischemic stroke or TIA to either ASA + ER-DP treatment or ASA monotherapy within 24 h following the event. After 7 days, all patients were treated for up to 90 days with ASA + ER-DP. MCP-1 was determined from blood samples taken from 425 patients on admission and day 8. The change in MCP-1 from admission to day 8 did not differ between patients treated with ASA + ER-DP and ASA monotherapy (p > 0.05). Comparisons within MCP-1 baseline quartiles indicated that patients in the highest quartile (>217-973 pg/mL) showed improved outcome at 90 days if treated with ASA + ER-DP in comparison to treatment with ASA alone (p = 0.004). Our data does not provide any evidence that treatment with ASA + ER-DP lowers MCP-1 in acute stroke patients. However, MCP-1 may be a useful biomarker for deciding on early stroke therapy, as patients with high MCP-1 at baseline appear to benefit from early treatment with ASA + ER-DP.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>22942727</pmid><doi>10.3390/ijms13078670</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | acetylsalicylic acid (ASA) Adult Aged Aged, 80 and over antithrombotic therapy Aspirin Aspirin - administration & dosage Biomarkers Biomarkers - blood Body mass index Brain Ischemia - blood Brain Ischemia - drug therapy Chemokine CCL2 - blood dipyridamole Dipyridamole - administration & dosage Drug Therapy, Combination Female Follow-Up Studies Humans Ischemia ischemic stroke Leukocytes Male Middle Aged monocyte chemoattractant protein-1 (MCP-1) neuroprotection Platelet Aggregation Inhibitors - administration & dosage Proteins Stroke Stroke - blood Stroke - drug therapy Time Factors Traumatic brain injury |
title | Monocyte chemotactic protein-1 as a potential biomarker for early anti-thrombotic therapy after ischemic stroke |
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